[The role of ATP-receptor in controlling the urinary bladder and urethral function in rats].

BACKGROUND: The detrusor contraction involves an atropine resistant, nonadrenergic noncholinergic (NANC), component. Since adenosine triphosphate (ATP) has been proposed as a NANC transmitter, the role of ATP-receptors in the lower urinary tract was examined. MATERIALS AND METHODS: The isovolumetric bladder contractions and the urethral pressure were monitored after intra-arterial administration of ATP analogues and other drugs in 52 female SD rats under intraperitoneal urethane anesthesia. RESULTS: alpha beta metATP induced a rapid, phasic increase of the maximal bladder pressure immediately after the drug administration, which was followed by a decrease during the P 2 X-purinoceptor desensitization period, but it did not affect the resting bladder pressure. RB-2 did not affect both the maximal bladder pressure and the resting bladder pressure. As for the urethral functions, alpha beta metATP induced a decrease of the resting urethral pressure during the P 2 X-purinoceptors desensitization period, while RB-2 induced a increase of the resting urethral pressure in contrast. ATP, alpha beta metATP and RB-2 did not changed the maximal urethral relaxation. CONCLUSION: The results will indicate that ATP produces detrusor contractions through the P 2 X-purinoceptor. Although ATP dose not affect urethral relaxation during voiding phase, it controls the urethral tone during collecting phase by both the excitation of P 2 X-purinoceptor and the inhibition of P 2 Y-purinoceptor.